Calcineurin is a calcium and calmodulin dependent serine/threonine protein phosphatase.
Calcineurin activates the T cells of the immune system and can be blocked by inhibiting drugs.
Calcineurin and Inhibitors are highly effective in preventing acute kidney transplantation rejection but have inherent nephrotoxicity.
Calcineurin activates nuclear factor of activated T cell cytoplasmic, a transcription factor, by dephosphorylating it.
The activated nuclear factor of activated T cytoplasmic is then translocated into the nucleus, where it upregulates the expression of interleukin 2 (IL-2).
Calcineurin inhibitors in lupus nephritis have two separate impacts on calcineurin activity: immunomodulatory effects on T-cells and stabilization of the podocyte.
Inhibition of calcineurin in T cells prevents nuclear factor of activated T cells from moving to the nucleus, which reduces the transcription of genes encoding inflammatory cytokines.
This decreases lymphocyte proliferation and T-cell mediated responses.
Calcneurin inhibitors prevents the dephosphorylation of synaptopodin in the podocyte, preserving the cytoskeleton’s stabilizing function and lowers proteinuria.
Interleukin 2 in turn, stimulates the growth and differentiation of the T cell response.
Calcineurin is the target of a class of drugs called calcineurin inhibitors, which include cyclosporine, voclosporin, pimecrolimus and tacrolimus.
Calcineurin Inhibitors, inhibit early activation of T cells.
Calcineurin activates the T cells of the immune system and can be blocked by inhibiting drugs.
Calcineurin inhibitors, such as cyclosporine and tacrolimus, inhibit cell responsiveness to mast cell products and inhibit T cell activity.
Calcineurin inhibitors are used to suppress the immune system in organ allotransplant recipients to prevent rejection of the transplanted tissue.
Calcineurin inhibitors in lupus nephritis have two separate impacts on calcineurin activity: immunomodulatory effects on T-cells and stabilization of the podocyte.
Inhibition of calcineurin in T cells prevents nuclear factor of activated T cells from moving to the nucleus, which reduces the transcription of genes encoding inflammatory cytokines.